neuropsychiatric aspects of traumatic brain injury
TRANSCRIPT
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Neuropsychiatric aspects of Traumatic Brain Injury
By – Dr. Azfer Ibrahim
J.N.M.C, A.M.U
ALIGARH
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Introduction• TBI refers to any external mechanical force acting on
the brain which may cause temporary or permanent dysfunction
• TBI can be Open / Closed ;
• Focal / Diffuse
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Epidemiology
• The annual incidence of head trauma in the United States is approximately 2 million per year.
• Of these patients, 500,000 will probably require hospitalization, and about 80,000 will suffer from some level of chronic disability
• Frankowski RF: Descriptive epidemiologic studies of head injury in the United States: 1974–1984. Adv Psychosom Med 1986; 16:153–172
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• Men are injured twice as frequently as women, with the risk of fatal head injury being four times greater.
• The incidence of head injury increases to peak from ages 15 to 25, thereafter falling off, only to rise again in later years.
• Capruso DX, Levin HS: Neuropsychiatric aspects of head trauma,in Comprehensive Textbook of sychiatry, Vol 1. Edited by KaplanHI, Saddock BJ. Baltimore, MD, Williams & Wilkins, 1995, pp207–220
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• In persons under 45 years of age, TBI is the leading cause of death and disability, with an overall mortality rate of 25/100,000.
• Motor vehicle accidents are the most common cause of HI (50%),
Falls (21%),
violence (12%),
injuries from sports or recreational activities (10%).
• McAllister TW: Neuropsychiatric sequelae of head injuries. Psychiatr Clin North Am 1992; 15:395–413
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Risk Factors for Neuropsychiatric Disorders
• Increasing age• Arteriosclerosis• Alcoholism• Premorbid personality• Marital discord• Poor interpersonal relationships• Problems at work• Financial instability
Lishman WA: Physiogenesis and psychogenesis in the postconcussional syndrome. Br J Psychiatry 1988; 153:460–469
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Mechanisms of TBI
• Mechanical forces applied to the skull and transmitted to the brain.
• This may lead to focal and/or diffuse brain damage.
• Focal lesions direct blow to the head
brain laceration contusion
intracerebral hemorrhagesubarachnoid or SDHischemic infarct
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• Diffuse brain injury also results from the differential motion of the brain within the skull, causing a shearing and stretching of the axons.
• This can produce a wide spectrum of injuries, ranging from brief physiological disruption to widespread axonal tearing, called diffuse axonal injury (DAI).
• 14. Kwentus JA, Hart RP, Peck ET, et al: Psychiatric complications of closed head trauma. Psychosomatics 1985; 26:8–15
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• In addition to brain damage occurring at the time of the impact, secondary damage from several processes may occur during the recovery period.
• Hypoxia• Anemia• Metabolic abnormalities• Hydrocephalus• Intracranial hypertension• Fat embolism• SAH
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• Other delayed effects include – :
Release of excitatory amino acids Oxidative free-radical production Release of arachidonic acid -metabolites
Disruption of neurotransmitters like monoamines and serotonin
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Neurobiological changes
• Abnormality in glutamate pathway.
• Abnormality in cholinergic neuronal activity.
• Abnormality in ascending biogenic amine pathway.
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• Clinical evidence :
– CSF increase glutamate after TBI
– Glutamate antagonists have shown beneficial effects in experimental model
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• Clinical Evidences :
– Reduction in cholinergic transmission in hippocampal & neocortical areas observed after TBI.
– Dysfunction of septohippocampal cholinergic pathway is observed in experimental models which has significant role in posttraumatic cognitive and behavioral deficit.
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• Clinical evidences :
– Circulating level of catecholamine has significant correlation of TBI severity.
– Increased serotonegic & NA metabolites in CSF.
– Dysregulation of mesolimbic & mesocorticaldopaminergic pathway give rise to manic and hypomanic syndromes.
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Lobe functions
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Neuropsychiatric Sequelae of TBI
• Disorders of mood
• Cognition
• Behavior.
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• Cognitive deficit has been variously classified as
-delirium
-dementia due to HI
- Amnestic disorder due to HI
-or intellectual impairment
• 18. Lishman WA: The psychiatric sequelae of head injury: a review. Psychol Med 1973; 3:304–318
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• The behavioral problems associated with TBI have been the most difficult to classify.
• The signs and symptoms of the frontal and temporal lobe damage have been variously classified as frontal and temporal lobe syndromes,aggressive disorders, and personality changes.
• 18. Lishman WA: The psychiatric sequelae of head injury: a review.Psychol Med 1973; 3:304–318
• 2. Capruso DX, Levin HS: Neuropsychiatric aspects of head trauma,in Comprehensive Textbook of Psychiatry, Vol 1. Edited by KaplanHI, Saddock BJ. Baltimore, MD, Williams & Wilkins, 1995, pp207–220
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Cognitive Deficits
• Impairment of arousal
• Attention
• Concentration
• Memory
• Language
• Executive function.
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• Loss of memory may be for both verbal and nonverbal skills.
• Disturbances of executive functioning include poor planning
organizing
sequencing
set-shifting
with impaired judgment and impulse control.
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• The first is the period of loss of consciousness or coma, which occurs soon after injury.
• The second phase is characterized by a mixture of cognitive and behavioral abnormalities, such as agitation, confusion, disorientation, and alteration in psychomotor activity.
• This period is associated with inability to recall events, sequence time, and learn new information.
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• The first two phases, which last anywhere from a few days to 1 month after injury, are a form of posttraumatic delirium.
• What follows is a 6–12 month period of rapid recovery of cognitive function, followed by plateauing of recovery over 12–24 months subsequent to the injury.
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• The fourth phase is characterized by permanent cognitive sequelae.
• Includes problems with speed of information-processing, attention and vigilance, short- and long-term memory deficits, verbal and nonverbal deficits, and problems with executive functions and mental inflexibility.
• This phase has also been described as
“dementia due to head trauma.”
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Treatment
• Multidisciplinary
• Includes - pharmacotherapy
physical therapy
occupational therapy
recreation therapy
speech therapy
vocational rehabilitation.
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Std. neuropsychological test battery
• Processing speed
– Wechsler Adult Intelligence Scale – IV
• Memory
– Rey Auditory Verbal Learning
– Brief visuospatial memory test
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• Executive Functioning and Decision Making
– Trail making test
– Controlled oral word association
– Color word interference
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• Cognitive rehabilitation is also important, especially during the first 6 months after injury, and involves techniques to retrain the patient in specific domains by providing a series of mental stimuli, tests, and activities.
• 22. Wilson BA: Cognitive rehabilitation: how it is and how it might be. J Int Neuropsychol Soc 1997; 3:487–496
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• Dopaminergics or psychostimulants may improve deficits of arousal, poor attention, concentration, and memory.
• Methylphenidate and dextroamphetamine are the commonly used psychostimulants.
• Increase catecholamine activity by blocking the reuptake of NE and dopamine.
• 23. Karli DC, Burke TD, Kim HJ, et al: Effects of dopaminergic combinationtherapy for frontal lobe dysfunction in traumatic brain injury rehabilitation. Brain Inj 1999; 13:63–68
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• Numerous case reports are available on the efficacy of dopaminergics in treating cognitive symptoms.
• Amantadine, bromocriptine, and levodopa are commonly used dopaminergic agents.
• 24. Van Reekum R, Bayley M, Garner S, et al: N-of-1 study: amantadine for the amotivational syndrome in a patient with TBI. Brain Inj 1995; 9:49–53
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• Cholinergic agents such as those developed to treat dementia are also showing promise in treating these deficits.
• 27. Taverni JP, Seligei G, Lichtman SW: Donepezil-mediated memory improvement in traumatic brain injury during post-acute rehabilitation. Brain Inj 1998; 12:77–80
• 28. Goldberg E, Gerstman LJ, Mattis S, et al: Effects of cholinergic treatment on posttraumatic anterogradeamnesia. Arch Neurol 1982; 39:581
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Mood Disorders
• Adolf Meyer, in 1904, referred to these symptoms as “traumatic insanities”.
(Meyer A: The anatomical facts and clinical varieties of traumatic insanity.
Am J Insanity 1904; 60:373–441)
• Depression and mania are common after TBI.
• Major depression occurs in approximately – First year post TBI 25 – 50%
– Life time 26-64%
Koponen S, Taiminen T et al (Am J Psychiatry 2000)
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• Depressive disorders were significantly more frequent among pts. of TBI than in pts. With orthopaedic injury. (Robinson RG, George RE. Arch Gen Psychiatry 2004)
• Approx. half of the pts. (53.1%) developed
major depression during first year of TBI. (Gould TR, Ponsfold JL Psychol Med 2011)
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• Feelings of loss, demoralization, and discouragement seen soon after injury are often followed by symptoms of persistent dysphoria.
• Fatigue, irritability, suicidal thoughts, anhedonia, disinterest, and insomnia are seen in a substantial number of patients 6–24 months or even longer after TBI.
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• Psychological impairments in excess of the severity of injury and poor cooperation with rehabilitation are strong indicators of a persistent depressive disorder.(Kraus MF: Neuropsychiatric sequelae: assessment and pharmacologic intervention, in Traumatic Brain Injury, Vol 14. Edited by Marion DW. New York, Thieme Medicine Publishers, 1999, pp 173–185)
• Clinical and research studies have also shown that poor premorbid level of functioning and past history of psychiatric illness are major risk factors for depression.
• Fedoroff JP, Starkstein SE, Forrester AW, et al: Depression in patients with traumatic brain injury. Am J Psychiatry 1992; 149:918–923
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• The mechanism of depression following head injury is probably due to disruption of biogenic amine-containing neurons as they pass through the basal ganglia or frontal-subcortical white matter.
• Starksein SE, Robinson RG, Price TR: Comparison of cortical and subcortical lesions in the production of poststroke mood disorders.Brain 1987; 110:1045–1059
• The presence of left dorsolateral frontal and left basal ganglia lesions is associated with an increased probability of developing major depression.
• Fedoroff JP, Starkstein SE, Forrester AW, et al: Depression in patients with traumatic brain injury. Am J Psychiatry 1992; 149:918–923
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Treatment
• Similar to the treatment of MDD.
• Antidepressants
• Psychostimulant
• ECT
• The choice of medications must be influenced by their side-effect profile.
• Agents such as serotonin-specific reuptake inhibitors (SSRIs) are safe and well tolerated.
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• SSRIs are useful in the treatment of depression, mood lability, and impulsivity.
• However, no placebo-controlled, double-blind case series is available to demonstrate the efficacy of these medications.
• Sertraline and citalopram are favoured in light of their benefecial effects,relatively limited side effects & short half lives.
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• Tricyclics and monoamine oxidase inhibitors are generally not preferred in the treatment of TBI patients because of their anticholinergicside effects and drug–food interactions, respectively.
• Psychostimulants and even the dopaminergicscan be helpful in these cases, as they have an antidepressant effect.
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• Methylphenidate has been compared to sertraline in a small double blind parallel group study.
• Both agents improved depression but methylphenidate not sertraline, also improved neuropsychological performance.
• Lee H, Kim SW, Kim JM, et al. Hum Psychopharmacol 2005
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• ECT is a highly effective mode of treatment for TBI patients refractory to antidepressants– Lowest possible enrgy level
– Adequate seizure duration (more than 20 s)
– Increased spacing of T/t (2-5days)
– Using pulsatile current
– Max. 4-6 T/t
– Non dominant U/L ECT.
• Ruedrich SL, Chu CC, Moore SL: ECT for major depression in a patient with acute brain trauma. Am J Psychiatry 1983; 140:928– 929
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• rTMS (repetitive transcranial magnetic stimulation)
• tDCS (transcranial direct current stimulation)
• Vagal nerve stimulation
• Deep brain stimulation
– No evidence
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Manic, hypomanic & mixed Ds
• Less common than depression but much more common than in the general population.
• It is seen in about 6.5 - 9% of patients.• Right ventral frontal & basotemporal injury.• Episodes were short lasting (less than 2
months).
• Jorge RE, Robinson RG, Starksein SE, et al: Secondary mania following traumatic brain injury. Am J Psychiatry 1993; 150:916–921
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• Changes in mood, sleep, and activation may manifest as irritability, euphoria, insomnia, agitation, aggression, impulsivity, and even violent behavior.
• Positive family history of affective disorder and subcortical atrophy prior to TBI are added risk factors.
• Stuart JW, Hemsath RN: Bipolar illness following TBI treatment with lithium and carbamazepine. J Clin Psychiatry 1988; 49:74–75
• Robinson RG, Boston JD, Starkstein SE, et al: Comparison of mania and depression after brain injury: causal factors. Am J Psychiatry 1988; 145:172–178
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Treatment
• T/t with anticonvulsants such as carbamazepineor valproate may be more effective than lithium, which is not specific to the neuropathology of TBI and may worsen cognitive impairment. (Kraus MF:
Neuropsychiatric sequelae: assessment and pharmacologic intervention, in Traumatic Brain Injury, Vol 14. Edited by Marion DW. New York, Thieme Medicine Publishers, 1999, pp 173–185)
• Valproate may exacerbate cognitive impairment in some but it appears less likely to do so than either carbamazepine or lithium. (Dikmen SS, MachamerJE. Neurology 2000)
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• Atypical antipsychotics
– Risperidone,olanzapine,ziprasidone
• Newer anticonvulsants
– lamotrigine,oxcarbazepine
Psychotherapies, ECT & brain stimulation techniques
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Anxiety Disorders
• Anxiety disorders are common in patients with TBI and range in frequency from 11%–70%.
• All variants of anxiety disorders are seen
– GAD
– PD
– phobic disorders
– PTSD
– OCD• Paul SM: Anxiety and depression: a common neurobiological substrate. J Clin
Psychiatry 1988; 49(suppl):13–16
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• TBI patients often experience generalized “free-floating” anxiety associated with persistent worry, tension, and fearfulness.
• Increased activity of the aminergic system and decreased activity of the GABA inhibitory network is the proposed mechanism for the clinical manifestation of anxiety.
• Jorge RE, Robinson RG, Starkstein SE, et al: Depression and anxiety following TBI. J Neuropsychiatry Clin Neurosci 1993; 5:369– 374
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• Right-hemispheric lesions are more often associated with anxiety disorder than left-sided lesions.(Paul SM: Anxiety and depression: a common neurobiological substrate. J Clin Psychiatry 1988; 49(suppl):13–16 )
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PTSD
• An anxiety disorder that results from exposure to a traumatic event that poses actual or threatened death or injury.
• Presence of trauma related symptoms.
• Reexperiencing of the traumatic event
• Persistence symptoms of increased arousal
• Duration 1 month
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• Controversy• It has been proposed that loss of consciousness and
posttraumatic amnesia after traumatic brain injury prevent the development of PTSD in moderate and severe traumatic brain injury.
• On the other hand, other investigators reported that PTSD is a relatively frequent complication of traumatic brain injury.
• They argue that traumatic brain injury patients can encode and retrieve trauma memories at an implicit level and that these memories can influence ongoing emotions and behaviors.
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Treatment
• Anecdotal evidence suggests that antidepressants such as SSRIs
• opioid antagonists such as naltrexone (Tennant FS:
Naltrexone treatment for PCS. Am J Psychiatry 1987;144:813–814)
• and buspirone (Gualiteri CT: Buspirone: neuropsychiatric effects. J
Head Trauma Rehabil 1988; 6:90–92)
• are promising in the treatment of anxiety disorders.
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• Benzodiazipines (Preston GC, Ward CE, Broks P, et al: Effects of lorazepam on
memory attention and sedation in attention by Ro15-1788. Psychopharmacology 1989; 97:222–227)
• and antipsychotics Feeney DM, Gonzalez A, Law WA: Amphetamine,
haloperidol,and experience interact to affect rate of recovery after motor cortex injury. Science 1982; 217:855–857)
should be avoided because they cause memory impairment, disinhibition, and delayed neuronal recovery.
• Behavioral therapy and psychotherapy.
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Psychosis
• A review of the literature by Davison and Bagley revealed that 0.7%–9.8% of pts. with TBI develop schizophrenia-like psychosis.
• Most of these pts. do not have a family history of schizophrenia.
(Davison K, Bagley CK: Schizophrenia-like psychosis associated with organic disorder of the CNS. Br J Psychiatry 1969; 4(suppl):113–184 )
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• Other studies have shown that the incidence of head injury pre-dating psychotic symptoms in a population of patients with schizophrenia is about 15%.
• Nasrallah HA, Fowler RC, Judd LL: Schizophrenia-like illness following head injury. Psychosomatics 1981; 22:359–361
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• Psychotic symptoms following TBI often manifest as frank delusions, hallucinations, and illogical thinking.
• They may also be associated with symptoms of agitation, ideas of reference, grimacing, silly giggling, expression of odd ideas, regression, and impulsive aggressiveness.
Thompsen C: Late outcome of very severe blunt head trauma: a 10–15-year follow-up. J Neurol Neurosurg Psychiatry 1984; 47:260–268
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Common delusions
• Capgras syndrome (loved ones are replaced by impostors)
• Reduplicative paramnesia (familiar place such as home is duplicated in another locations)
• Cotard syndrome (being dead or dying)
• The psychotic features may be acute or chronic, transient or persistent, and may or may not be associated with mood disturbances.
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Treatment
• More susceptible for ADRs. such as sedation, anticholinergic, EPS.
• Seizure should be considered.
• Trial of anticonvulsant before starting antipsychotic could be considered.
• Neuroleptics, if administered, should be given in low doses, as animal studies have shown impaired neuronal recovery.
• Levine DN, Finkelstein S: Delayed psychosis after right temporal– parietal stroke or trauma: relation to epilepsy. Neurology 1982; 32:267–273
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• when there is a suggestion of left-temporal involvement, there may be benefit from the use of an anticonvulsant.
• Delusional-type symptoms that seem more related to cognitive and behavioralimpairments from frontal lobe dysfunction can benefit from dopaminergics.
• Nonpharmcological T/t.
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Apathy
• 10 % of pts. tend to have apathy without depression, and 60% have some degree of apathy and depression following TBI.58
• General reduction in motivation - Marin
• Apathy refers to a syndrome of disinterest, disengagement, inertia, lack of motivation, and absence of emotional responsivity.
• Kant R, Duffy JD, Pivovarnik A: The prevalence of apathy following head injury. Brain Inj 1988; 12:87–92
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• Apathy is not listed as a specific syndrome or symptom in either DSM-5 or ICD -10.
• The negative affect and cognitive deficits seen in patients with depression are not seen in patients with apathy.
• Apathy may be secondary to damage of the mesial frontal lobe.
• Duffy JD, Campbell JJ: The regional prefrontal syndromes: a theoretical and clinical overview. J Neuropsychiatry Clin Neurosci 1994; 6:379–387
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• Apathy evaluation scale (AES) – Marin et al
• It often responds well to either– Psychostimulants (Methylphenidate)
– Dopamine agonist (amantadine,selegiline)
• Van Reekum R, Bayley M, Garner S, et al: N-of-1 study: amantadine for the amotivational syndrome in a patient with TBI. Brain Inj 1995; 9:49–53
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Behavior Dyscontrol Disorder
• Major variant. A complex syndrome, with mood, cognitive, and behavioral manifestations is seen in a number of patients after TBI. (Gerring JP: Psychiatric
sequelae of severe closed head injury. Pediatric Review 1986; 8:115–121)
• This occurs in both the acute and chronic stages after TBI.
• Its prevalence is about 5%–70%.(Silver JM, Yudofsky SC:
Aggressive disorder, in Neuropsychiatry of Traumatic Brain Injury. Edited by Silver JM, Yudofsky SC, Hales RE. Washington, DC, American Psychiatric Press, 1994, pp 313–353)
• Major feature of the syndrome is dyscontrol of emotion, behavior, and cognition.
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Mechanism
Both focal and diffuse brain injury
disruption of neuronal network
creating lapses in cognitive functioning
and coarsening of behaviour
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• Focal damage to the orbital–frontal area causes disinhibition, and injury to the dorsal convexity of the frontal lobe causes dysexecutive symptoms. Duffy JD, Campbell JJ: The regional
prefrontal syndromes: a theoretical and clinical overview. J Neuropsychiatry ClinNeurosci 1994; 6:379–387 60
• Damage to the temporal lobes causes emotional lability and memory problems.Gualtieri CT: Neuropsychiatry and Behavioral Pharmacology. New York, Springer-Verlag, 1991
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Treatment
• A multidisciplinary approach.
• They would benefit from a combination of environmental modification strategies,– Behavioral therapy (including positive and
negative reinforcement)
– vocational training
– supportive psychotherapy
– family therapy.
• Epstein NB, Bishop DS: Problem-centered systems therapy of the family, in Handbook of Family Therapy. Edited by Gurman A, Kniskern D. New York, Brunner/Mazel, 1981, pp 444–482
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• Pharmacotherapy
– dopaminergic agents
– psychostimulants,
– opioid antagonists,
– SSRIs,
– high-dose betablockers,
– buspirone,
– trazodone, and anticonvulsants.
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Minor variant Behavior dyscontroldisorder
• or post-concussion syndrome (PCS), is the most commonly diagnosed entity following TBI.
• The syndrome is poorly defined and has been a source of controversy for a number of years.
• It refers to a cluster of signs and symptoms that often follows mild TBI but can occur with injury of any severity.
• Evans RW: The post-concussion syndrome and the sequelae of mild head injury. Neurol Clin 1992; 10:815–847
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• The management of this disorder should be practical and holistic.
• Education and support of patients and family members should be associated with supportive and behavioral psychotherapy, occupational and vocational intervention, and social skills training.
• If the patient is experiencing significant cognitive or emotional difficulties, he or she should be evaluated for an affective or anxiety disorder and treated appropriately.
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Sleep disturbances
• Upto 68%
• Sleep hygiene
• Hypnotic & BZD not recommended for long term
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CONCLUSION
• Patients with traumatic brain injury are often referred to as “the walking wounded,” because a number of them have persistent neuropsychiatric sequelae.
• Even though they appear physically “normal,” they are disabled personally, socially, and occupationally.
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• Ideally, treatment of these patient should involve a multidisciplinary approach, with the neuropsychiatrist working in close collaboration with the patient, family, neurologist/neurosurgeon, psychologist, social worker, and the staff of community groups such as the local chapter of the brain injury association.